Third set of review questionsSome of these are redundant with previously posted review questions, but all relate to important concepts that are worth repeating.
People with type A blood do not make antibodies whose binding sites fit the type A antigen. Explain what is true or false about each of the following possible explanations. Are any of them completely true?
b) These people's lymphocytes recognize A antigens as being "self"?
c) The genes for type A blood prevent the VDJ recombination mechanism from producing antibody binding sites that fit the type A antigen?
d) Because it would kill anyone to make antibodies whose binding sites fit any of their own antigens, therefore natural selection has eliminated the ability to make antibodies that specifically bind to any of your own antigens?
e) Because all lymphocytes whose binding sites fit "self" antigens are induced to die during embryonic development?
f) Because the presence of type A blood cells during embryonic development causes death or inactivation of all lymphocytes whose VDJ recombination mechanism is capable of producing binding sites whose shape fits the A antigen?
g) Because the presence of type A blood cells during embryonic development causes death or inactivation of all lymphocytes whose VDJ recombination mechanism has produced a binding site whose shape fits the A antigen?
When the shape of an embryonic lymphocyte's binding site binds tightly to a certain antigen:
b) That means that the antigen must be "non-self"
c) That means that the antigen cannot be "self"
d) That means that the antigen cannot be "non-self"
e) None of the above?
The method by which the immune system detects that an antigen must be "self" is
b) That many different lymphocytes have binding sites that fit that antigen?
c) That all "self" antigens bind to certain special antibodies, that mark them as self?
d) That all "self" antigens get weeded out during embryonic development.
e) None of the above.
Note: In the following question more than one can be correct:
Which of the following might be a cause of an autoimmune disease?
b) If some "self" proteins fail to be marked as self?
c) If certain "self" proteins are only present in parts of the body where no lymphocytes ever normally go?
d) If the VDJ recombination process continues to occur after embryonic development?
e) If the genes for certain "self" genes have unusually high mutation rates?
e) If a woman's two X chromosomes each codes for differently shaped variants of a certain enzyme?
Do you remember the time-lapse video of magnetic resonance scans of the brain of a person with multiple sclerosis? (This is at the beginning of the April 20 lecture video). Which of the following correctly describes the time and space pattern of lesion formation?
b) Lesions form at one location, then disappear, and other lesions then form at other locations?
c) Once having developed at a certain location, lesions never disappear?
d) Lesions are always the same size?
e) Lesions are always long and thin?
What tentative conclusions, or theories, would be supported by each of the descriptions above, if it were true?
w) Maybe swarms of anti-myelin lymphocyte, like locusts, attack one place and then another?
x) Maybe anti-myelin lymphocytes never leave an area, once they attack it?
y) Maybe damage to myelin can never be repaired?
z) Maybe anti-myelin lymphocyte are themselves damaged when they attack an area of the brain?
Which of the following would (or could) be a cure for multiple sclerosis?
b) Induction of apoptosis in any lymphocyte which enters the interior of the brain?
c) Induction of apoptosis in any lymphocyte which binds to oligodendrocytes?
d) Induction of apoptosis in all lymphocytes which bind to any form of myelin?
e) Stimulation of much faster repair of damaged oligodendrocytes?
f) Chemotactic attraction of anti-myelin lymphocytes into surgically implanted sponges?
g) Mono-clonal antibodies whose binding sites selectively bind to the binding sites of anti-myelin lymphocytes?
h) Mono-clonal lymphocytes whose binding sites fit the binding sites of anti-myelin lymphocytes?
i) Poisonous chemicals, parts of which have shapes very similar to myelin? j) Blockage of apoptosis in oligodendrocytes?
k) Non-specific supression of the whole immune system.
Which kinds of animals control which sex an individual will become by the temperature of the egg during early development?
A fly with only one X chromosome per cell, and no Y chromosome will be...?
In both cases, explain why (in terms of their normal method of sex determination?
If a certain form of cancer is caused by an enzyme that is not made in normal cells, can you explain why this cancer is treated by chemicals that selectively block this abnormal enzyme?
If a certain form of cancer is caused by excess production of a protein that blocks apoptosis, can you explain why this cancer is treated by chemicals that selectively damage DNA?
Failure of epithelial sheets to fuse with each other, normally, during embryonic development is a major cause of what?
List as many examples as you can in which anatomical abnormalities result from failure of particular epithelial tissues to fuse with each other.
Invent a birth defect that could, in principle, be caused by failure of certain epithelia to fuse (but as far as you know, doesn't actually occur).
If you surgically removed the insect gland that secretes juvenile hormone, would that prevent molting. Would it cause metamorphosis?
Compare and contrast hormonal control of metamorphosis of frogs versus butterflies.
Invent and describe a molecular mechanism for co-linearity of hox gene expression. In other words, a mechanism capable (in principle) of causing the locations and times of transcription of closely linked hox genes to occur in the same spatial sequence in the embryo as the spatial sequence in which these hox genes are arranged along their chromosomes.
Based on your theory, what abnormality of hox gene transcription ought to be caused by reversing the locations on their chromosomes of two or more hox genes?
Invent and describe at least one other testable prediction of your theory of co-linearilty.
The synthesis of embryonic hemoglobin, fetal hemoglobin, and then adult hemoglobin is analogous in what way to the transcription of hox genes?
Suppose that a certain transciption factor (protein) is too large to diffuse either out of cells or into other cells, but that cells can detect the amounts of this protein in cells adjacent to them, then explain how these properties can nevertheless produce what looks exactly like a diffusion gradient of the protein (even though it can't diffuse).
. As a variation of the preceding question, what if cells could only compare whether neighboring cells contain higher or lower concentrations (than they, themselves contain)? Explain whether that would be sufficient to mimic diffusion gradients.
Another variation of this type of question: Suppose that the transcription factors coded for by hox genes cannot themselves diffuse from one cell to another, but that each of them stimulates synthesis of different amounts of a protein that can diffuse from cell to cell, and that can alter amounts of transcription of different hox genes: explain how this set of properties could produce spatial patterns of hox gene transcripts that mimic diffusion gradients.
Yet another variation on this type of "how to to produce what looks like a diffusion gradient"!
As you may remember, each finger transcribes a different combination of hox genes:
Ring finger: Hox-D9, Hox-D10,
Middle finger: Hox-D9, Hox-D10, Hox-D11,
Index finger: Hox-D9, Hox-D10, Hox-D11, Hox-D12
Thumb: Hox-D9, Hox-D10, Hox-D11, Hox-D12, Hox-D13,
Try to figure out how tissues would need to change which hox genes they transcribe, based on what hox genes are transcribed by adjacent cells, so as to predict and explain the triple branching pattern that occurs.
MORE QUESTIONS WILL BE POSTED.
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